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Double-Barreled Assault by Aldosterone and Salt on the Heart

机译:醛固酮和盐对心脏的双管攻击

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Idosterone, a mineralocorticoid hormone secreted by A the adrenal zona glomerulosa, is generally regarded as the end product of the renin-angiotensin-aldosterone system. Aldosterone is a major regulator of body fluid and electrolyte homeostasis by virtue of its classic actions at renal collecting duct principal cells, mediated by miner- alocorticoid receptors (MR), to induce sodium (Na*) and water reabsorption and potassium (K*) excretion. In ad- dition to these classic effects, aldosterone induces non- classical actions in both epithelial and nonepithelial tis- sues, including inflammation and fibrosis that lead to cardiac, vascular, and renal target organ damage. Indeed, a large body of evidence supports the concept that aldo- sterone induces deleterious effects on the cardiovascular system independently of both angiotensin II and blood pressure (1, 2).
机译:肾上腺带状肾小球A分泌的盐皮质激素荷尔蒙酮通常被认为是肾素-血管紧张素-醛固酮系统的终产物。醛固酮是矿物质和类固醇激素受体(MR)介导的对肾收集管主细胞的经典作用,是诱导钠(Na *)和水重吸收以及钾(K *)的主要作用,因此是体液和电解质稳态的主要调节剂。排泄。除上述经典作用外,醛固酮还可以在上皮和非上皮组织中引起非经典作用,包括导致心脏,血管和肾靶器官损害的炎症和纤维化。确实,大量证据支持醛固酮独立于血管紧张素II和血压而对心血管系统产生有害作用的概念(1、2)。

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